PSMD12 is a novel potential biomarker for lung adenocarcinoma and associated with prognosis in lung adenocarcinoma patients
摘要
This study aims to comprehensively evaluate the expression pattern of PSMD12 in lung adenocarcinoma (LUAD) and its impact on prognosis, and to explore its potential application value in the diagnosis and treatment of LUAD.
MethodsThis study employed bioinformatics analysis and molecular biology experiments to comprehensively investigate the expression pattern of the PSMD12 gene in LUAD and its association with LUAD patients’ clinical features. First, we evaluated the differential expression of PSMD12 in 44 different tumor types and its relationship with the prognosis of LUAD patients. GO, KEGG, and GSEA were used to analyze the function of PSMD12. Secondly, TIMER was applied to evaluated the relationship between PSMD12 gene expression and immune infiltration characteristics in LUAD patients. Finally, RT-qPCR, CCK-8, clone formation assay, wound healing assay, and Transwell assay were used to verify the effects of knockdown PSMD12 expression on the proliferation, migration, and invasion abilities of LUAD cells.
ResultsSurvival analysis results showed that high PSMD12 gene expression levels were significantly correlated with the poor prognosis of LUAD patients. The importance of PSMD12 in key metabolic pathways and disease processes such as neuroactive ligand-receptor interaction, taste and olfactory transduction, and steroid hormone biosynthesis was revealed. Immune infiltration analysis results showed that PSMD12 expression was negatively correlated with M2 macrophages, revealing the potential role of PSMD12 in regulating the immune microenvironment of LUAD. In vitro experiments verified the functional role of the PSMD12 in LUAD cells, indicating that knockdown of PSMD12 weakened the proliferation, migration, and invasion abilities of LUAD A549 and H1299 cells.
ConclusionsHigh expression of PSMD12 may be closely related to poor prognosis in LUAD patients and promotes the malignant progression of LUAD by enhancing the proliferation, migration, and invasion of LUAD cells.